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  • islet cell replication  (2)
  • B cell proliferation  (1)
  • Life and Medical Sciences  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 27 (1984), S. 464-467 
    ISSN: 1432-0428
    Keywords: Inbred mouse strains ; alloxan diabetes ; islet culture ; islet implantation ; islet cell replication ; autoradiographic labelling index ; proinsulin biosynthesis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Proliferation of islet cells may compensate for both an increased peripheral insulin resistance and islet cell destruction but the capacity for regeneration may be genetically determined. For the latter reason, glucose-stimulated islet cell replication was estimated in both inbred C57BL/6J (BL/6) and C57BL/KsJ (BL/Ks) mice. Islets isolated from both strains were exposed to high concentrations of glucose in vitro or in vivo for a prolonged time period. This was achieved either by culturing the islets free-floating in a high glucose concentration medium for 3 days or implanting the islets intrasplenically in insufficient numbers to cure alloxan-diabetic syngeneic recipients. In both strains high glucose concentration culture was found to increase the autoradiographic labelling index of the islets but the replicatory activity decreased with age. The proliferative rate of the islet cells of the BL/6 mice was about twice as high as that of the BL/Ks mice irrespective of age and glucose concentration. Likewise, the labelling index of intrasplenic BL/6 islets implanted into alloxan-diabetic mice was twice as high as that of the islets implanted into alloxan-diabetic BL/Ks mice. The replicatory activity of the latter islets did not differ statistically from that of islets implanted into non-diabetic control BL/Ks mice. No differences in the rates of proinsulin and total protein biosynthetic rates were observed between high glucose concentration-cultured islets of the two mouse strains. The present results indicate that the proliferative response of pancreatic islets to a prolonged glucose stimulation may be genetically determined. This may play a significant role in the development of different diabetic syndromes both in laboratory animals and man.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0428
    Keywords: Obese-hyperglycaemic mice ; isolated pancreatic islets ; islet transplantation ; serum glucose ; islet volume ; autoradiography ; islet cell replication ; immunocytochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Implantation of allogeneic pancreatic islets encapsulated in Millipore diffusion chambers has been reported to normalize the obese-hyperglycaemic syndrome in mice. In the present study, both young and adult ob/ob mice remained hyperglycaemic and gained weight after intrasplenic implantation of 500 isogeneic islets isolated from lean mice. Such islets normalized the elevated blood-glucose of alloxan-diabetic lean mice. Morphometric analysis of the intrasplenically implanted islets showed that the mean islet volume in the ob/ob mice was five times larger than that of the lean, non-diabetic mice. Immunocytochemical staining of the spleens showed an increased proportion of B-cells in the enlarged, intrasplenic islets in the ob/ob mice. Moreover, autoradiographical examination of these islets demonstrated the presence of several labelled cells. These results suggest that the growth of the implanted “lean” islets is due to extrapancreatic factors which stimulate islet cell replication in the obese-hyperglycaemic mouse.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 23 (1982), S. 525-528 
    ISSN: 1432-0428
    Keywords: Diabetes ; rat pregnancy ; islets of Langerhans ; B cell proliferation ; diabetic fetopathy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Since it has not been possible to reproduce, in the rat, the hyperplasia of the islets of Langerhans observed in the fetus in human diabetic pregnancy, the rate of proliferation of the endocrine pancreas of fetuses of manifest diabetic rats has been studied. Rats were rendered diabetic by streptozotocin injections before mating. At days 20 or 22 of gestation the pregnant rats were injected with colchicine and sacrificed at 1-h intervals. The mitotic indices of the fetal endocrine pancreas were determined and plotted against the time after colchicine injection. The production of new cells (i.e. the cell birth rate) was estimated from the slopes of the regression lines. On both days 20 and 22 of gestation, the cell birth rates of the endocrine pancreas of the fetuses of manifest diabetic mothers were only one-third of the control values obtained in normal, age-matched fetal pancreas (daily cell birth rate = 10%). This finding corresponds to the previous observation of a low B cell mass in the offspring of diabetic rats. The results indicate that the growth and development of the fetal endocrine pancreas is retarded in manifest diabetic pregnancy in the rat.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 128 (1986), S. 322-328 
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: We investigated the influence of transforming growth factor-β (TGF-β) on DNA synthesis in human fetal fibroblasts, as measured by the incorporation of [3H] thymidine and cell replication. In serum-free medium, without additional peptide growth factors, TGF-β had no action on thymidine incorporation. However, in the presence of 0.1% v/v fetal calf serum, TGF-β exhibited a bi-functional action on the cells. A dose-dependent stimulation of [3H] thymidine incorporation, and an increase in cell number, occurred with fibroblasts established from fetuses under 50 g body weight, with a maximum stimulation seen at 1.25 ng/ml. For fibroblasts from fetuses of 100 g or greater body weight, TGF-β caused a dose-related decrease in thymidine uptake with a maximal inhibition at 2.5 ng/ml, and a small decrease in cell number. When DNA synthesis was stimulated by the addition of somatomedin-C/insulin-like growth factor I, epidermal growth factor, or platelet-derived growth factor, their actions were potentiated by the presence of TGF-β on cells derived from fetuses under 50 g body weight, but inhibited on cells obtained from the larger fetuses wieghing more than 100 g. Similar results were found for changes in cell number in response to TGF-β when stimulated by SM-C/IGF I. The ability of TGF-β to modulate [3H] thymidine incorporation did not involve a change in the time required for growth-restricted cells to enter the S phase of the replication cycle. These data suggest that TGF-β may exert either a growth-promoting or growth-inhibiting action on human fetal connective tissues in the presence of other peptide growth factors, which is dependent on fetal age and development.
    Additional Material: 8 Ill.
    Type of Medium: Electronic Resource
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